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Twelve blood chemistry values, six haematological values and bodyweight were estimated for six-week-old specific-pathogen-free brown leghorns. Observations were based on 208 birds sampled from 11 groups. Subsequently the same values were estimated for specific pathogen free brown leghorns and broiler hybrids of differing ages. These estimates have been designated "comparison values" and were intended for reference use in clinical pathology. Results were compared with 14 "comparison value" estimated obtained previously for six-week-old commercial broiler hybrids. Haematological values varied with age and type of bird. Differences were observed between bird types in serum protein, serum cholesterol, uric acid, calcium and potassium levels and in weight. The significance of these differences is discussed.

SUMMARY1. Human subjects received intravenous infusions of adrenaline preceded by saline, phentolamine (an a-blocker) or either pronethalol or propranalol (fl-blockers), in different experiments.2. Clinical measurements of blood pressure and pulse rate confirmed that oc-or ,-blockade had been achieved.3. The rise in clotting factor VIII induced by adrenaline was blocked by pronethalol and propranalol but not by phentolamine. This indicated that the effect of adrenaline on factor VIII was mediated by f-receptors.

Adrenaline, isoprenaline and salbutamol were administered by intravenous infusion to human subjects. Isoprenaline was covered with practolol in an attempt to reduce the unpleasantness of the circulatory effects. Changes were recorded in pulse rate and blood pressure, and in blood levels of factors V, VIII, X, XI, and XII, platelet count, lactate, pyruvate, potassium and free fatty acids. Factor VIII was studied by clotting assays, by reactions with two rabbit antisera and two human antibodies, and by desulphated agarose chromatography. At the rate at which they were adiminstered, all three drugs increased the pulse rate by 20-40 beats/min. Factor VIII rose c. 2.5 X with adrenaline but only c. 1.5 X with isoprenaline and salbutamol; but other clotting factors did not alter. Chromatography provided no evidence of a change in the size of the molecule carrying factor-VIII clotting activity. The rate of clearance of the heightened plasma activity could not be shown to differ from that of "ordinary" factor VIII infused into haemophiliacs. The platelet count rose after adrenaline, fell after salbutamol and did not change significantly after isoprenaline. Among the biochemical responses, the only significant difference between the drugs was that lactate rose after adrenaline and salbutamol but did not change after isoprenaline. The rise in factor-VIII clotting activity after adrenaline is considered to represent a real increase in blood concentration, presumably by release of additional factor VIII from stores. The evidence suggests that this could be classified as a beta2 effect; and that the quantity which can be released is unrelated to the current plasma level. The rise in platelet count produced by adrenaline may be the resultant of an alpha-mediated rise due to contraction of the exchangeable splenic pool and a beta2-mediated fall, the alpha effect predominating.

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